More evidence that endothelial cells are not directly vulnerable to infection by SARS-CoV-2.

Endothelial dysfunction in COVID-19 is entirely indirect. https://twitter.com/covidblogger/status/1334618663102476289
Discussion thread on pericytes, nearby susceptible cells strongly suspected to mediate some of the damage. https://twitter.com/LucreSnooker/status/1334612932160856068?s=19
Discussion on infection of pulmonary megakaryocytes, i.e. platelet-forming cells, also strongly suspected of involvement. https://twitter.com/__ice9/status/1326285070827724806?s=19
Article on immunothrombosis, a pathological state in which the local inflammatory response particularly in the lungs drives endothelial dysfunction and progressive microthrombosis: https://twitter.com/MartinJuhl2/status/1330621187601391624?s=19
Discussion thread on influence of elevated plasma 5-HT (serotonin) in promoting endothelial dysfunction: https://twitter.com/farid__jalali/status/1310069518706696192?s=19
Further discussion of indirect causes of endothelial dysfunction in COVID-19, from a previous thread on the apparent resistance of endothelial cells to infection by SARS-CoV-2: https://twitter.com/__ice9/status/1326390661269090309?s=19
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